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Background and aims: Smoking tobacco has opposite effects on the different forms of inflammatory bowel disease (IBD). It predisposes to the development of Crohn's disease (CD) yet is associated with [...]

A. Moody [1] S. Fisher [1] M. Mirza [1] J. Hampe [2] S. Bridger [3] A Macpherson [3] S. Schreiber [2] A. Forbes [4] A. Cuthbert [1] C. Mathew [1] [...]

Four patients are described who presented with congenital finger contractures and arthropathy. There was synovial cell hyperplasia and giant cells but no inflammatory process. Radiographs showed flattening of the metacarpal and metatarsal heads and the proximal femoral ossification centres. In the oldest patient the process had subsided leaving slight contractures but severe impairment of hip mobility. In another the arthropathy was still prominent in the early teens. In a third, finger contractures had failed to respond to conservative or surgical measures. [ABSTRACT FROM PUBLISHER]

Changes in basal and stimulated acid secretion after duodenal ulcer healing have been previously shown to be influenced by the nature of the treatment. This study aimed to determine possible changes in nocturnal acid secretion on duodenal ulcer healing in patients treated with sucralfate or ranitidine. Nocturnal acid output and peak acid output in response to pentagastrin stimulation were studied in 20 patients before and after duodenal ulcer healing with sucralfate (n = 9) or ranitidine (n = 11). Details regarding cigarette smoking were obtained from each subject. Median 10 hour nocturnal acid output fell significantly (p less than 0.05) from 82.4 (29.1-188.3) mmol (median range) to 45.2 (14.7-144.4) mmol after healing with sucralfate, and rose significantly (p less than 0.05) from 54.7 (16.8-74.3) mmol to 86.2 (11.7-118.1) mmol after ulcer healing with ranitidine. Peak acid output fell from 39.6 (22.0-52.8) mmol/hour to 27.8 (13.8-38.2) mmol/hour (p less than 0.01) after healing with sucralfate and was unchanged after healing with ranitidine. There was no correlation between smoking and nocturnal acid output. These results provide further evidence that acid secretion decreases with sucralfate healing and remains the same or may even increase after ranitidine healing. [ABSTRACT FROM PUBLISHER]

Basal and maximum acid outputs were measured on two occasions in a group of 15 duodenal ulcer (DU) patients in remission. The initial study was carried out after a nocturnal acid collection, whereas the second was carried out in the conventional manner without preceding nocturnal aspiration. No difference in the basal acid output, concentration, or volume of secretion was found between the two study days. Maximum acid output on the other hand, was significantly (p < 0.02) reduced from 30.9 (14.2-41.2) mmol/h, median (+range), to 23.7 (8.1-33.7) mmol/h after overnight aspiration. The reduction in maximum acid output was attributable to a fall in the volume of gastric secretion from 280 (170-371) ml to 230 (142-280) ml. No fall in acid concentration was seen. We conclude that overnight gastric aspiration does not affect basal gastric secretion, but reduces the maximum acid output as a result of a reduced secretory volume. [ABSTRACT FROM AUTHOR]

Mothers with eating disorders can face additional challenges with infant feeding, and there is evidence they are likely to cease breastfeeding earlier than intended. However, there is little research exploring this. The present study used interpretative phenomenological analysis to explore the lived experience of infant feeding for mothers suffering from or recovering from an eating disorder. Semistructured interviews were conducted with six women-five who had breastfed and one who formula-fed. The women experienced two incompatible worlds-motherhood and an eating disorder. Tensions were sometimes resolved by reducing eating disordered behaviour alongside immersion in motherhood. Two participants did not find infant feeding particularly important for their journey into motherhood. Four recounted a positive shift in their relationship to their body through breastfeeding and felt their embodied experience of mothering provided a route out of eating disordered behaviour. However, doubts about their mothering and infant feeding capabilities could be amplified by feeling mistrusted by others and by the relative silence around eating disorders within maternity care services. Respectful dialogue with health care professionals was particularly valued where this occurred. Although long-term outcomes for the participants are unknown, the study suggests women with a history of eating disorders can form successful breastfeeding relationships and may be motivated to engage in collaborative risk assessment. However, they need support in managing emotional challenges. Training around eating disorders for maternity care professionals is likely to be useful for enhancing confidence in engaging mothers proactively to share concerns about eating, weight and body shape., (© 2024 The Author(s). Maternal & Child Nutrition published by John Wiley & Sons Ltd.)

Providing care and education for a patient on peritoneal dialysis (PD) requires that the nephrology nurse have knowledge and expertise in the PD access. This article provides information on types and placement of PD catheters, pre-placement and post-placement education and care, how to assess PD catheter exit site healing, and initial use of the PD catheter for access., Competing Interests: The author reported no actual or potential conflict of interest in relation to this continuing nursing education activity., (Copyright© by the American Nephrology Nurses Association.)

Background: Although informal end-of-life care is associated with significant physical and psychological morbidity for caregivers, few interventions have been developed to meet these needs. This study aimed to identify existing coping and support mechanisms among informal cancer caregivers in order to inform intervention development., Method: One-to-one semi-structured qualitative interviews were undertaken with 20 informal cancer caregivers of home palliative care patients., Results: Caregivers' existing coping strategies included distraction, mental stimulation, emotional release, looking for the positive aspects of caregiving, and disengaging from stressful thoughts. The majority of the participants described the importance of support and understanding form family and friends., Conclusions: The data suggests that feasible and acceptable interventions will be those that are targeted to caregivers to assist them in optimising existing coping strategies and support from family and friends.

Heritable predisposition to inflammatory bowel disease (IBD) has been demonstrated by epidemiological and genetic analysis. Linkage of IBD to broad regions of chromosome 16 has been established by analysis of multiple populations. NOD2, located on proximal 16q, was recently identified as an IBD gene. As the linkage regions on chromosome 16 are large, we have investigated the possibility that NOD2 is not the only IBD gene located on this chromosome. A high-density experiment using 39 microsatellite markers was performed to identify additional regions of association, and to indicate areas of interest for further investigation. A triple-peaked configuration of the linkage curve with peak logarithm of odds (lod) scores of 2.7, 3.2, and 3.1 was observed on proximal 16p, proximal 16q, and central 16q, respectively. The cohort was stratified by coding individuals carrying the NOD2 single nucleotide polymorphism (SNP)8 and SNP13 "unknown." Significance at the central peak, corresponding to the genomic location of NOD2, then decreased from 3.2 to 1.2. The maximal lod scores on the proximal p-arm (lod = 2.1) and central q-arm (lod = 2.6) changed only moderately. An exploratory association analysis (TRANSMIT) yielded a strong lead at D16S3068 (P = 0.00028). The region around this marker was further investigated by using anonymous SNPs. An associated haplotype containing three SNPs was identified (peak significance P = 0.00027, IBD phenotype). On stratification based on NOD2 genotype, this significance increased to P = 0.0001. These results confirm the importance of NOD2 and provide evidence for a second IBD gene located on chromosome 16p.

Background Genetic predisposition to inflammatory bowel disease (IBD) has been shown by epidemiological and linkage studies. Genetic linkage of IBD to chromosome 16 has been previously observed and replicated in independent populations. The recently identified NOD2 gene is a good positional and functional candidate gene since it is located in the region of linkage on chromosome 16q12, and activates nuclear factor (NF) kappaB in response to bacterial lipopolysaccharides. Methods We sequenced the coding region of the NOD2 gene and genotyped an insertion polymorphism affecting the leucine-rich region of the protein product in 512 individuals with IBD from 309 German or British families, 369 German trios (ie, German patients with sporadic IBD and their unaffected parents), and 272 normal controls. We then tested for association with Crohn's disease and ulcerative colitis. Findings Family-based association analyses were consistently positive in 95 British and 99 German affected sibling pairs with Crohn's disease (combined p<0.0001); the association was confirmed in the 304 German trios with Crohn's disease. No association was seen in the 115 sibling pairs and 65 trios with ulcerative colitis. The genotype-specific disease risks conferred by heterozygous and homozygous mutant genotypes were 2.6 (95% CI 1.5-4.5) and 42.1 (4.3-infinity), respectively. Interpretation The insertion mutation in the NOD2 gene confers a substantially increased susceptibility to Crohn's disease but not to ulcerative colitis.

Severe undernutrition has been associated with reduced secretions of gastric acid and pancreatic enzymes. This may be the result of an impaired gut mucosal response to food and primary gastric parietal and pancreatic acinar cell secretory dysfunction as a consequence of the poor nutritional state. To investigate the relative contributions of these factors, severely undernourished patients underwent enteral-meal-stimulated (ES; n = 7) or intravenous hormone (pentagastrin and cholecystokinin-8)-stimulated (HS; n = 12) gastric acid and pancreatic enzyme secretion before and after a period of nutritional support. Results were evaluated in comparison with normal healthy control subjects (ES = 7, HS = 10). In the control subjects, enteral-meal and cholecystokinin-8 stimulation resulted in similar outputs of the pancreatic enzymes amylase (2213 versus 2305 U/h), lipase (84.93 versus 118.6 U/h), and trypsin (498.9 versus 341.4 U/h), whereas acid output was significantly lower in the ES group (10.90 versus 25.53 mEq/h; P < 0.01). Compared with controls, malnourished groups had significantly reduced secretions of amylase (ES = 870.1 U/h, HS = 686.5 U/h; P < 0.02), lipase (ES = 30.68 U/h, HS = 25.96 U/h; P < 0.02), and trypsin (ES = 175.6 U/h, HS = 109.3 U/h; P < 0.01). The response to enteral-meal or CCK-8 stimulation was comparable. Gastric acid was similarly reduced in the undernourished patients (ES = 4.39 mEq/h, HS = 5.04 mEq/h; P < 0.01). After refeeding, secretion of amylase (ES = 2351 U/h, HS = 2228 U/h) and lipase (ES = 58.83 U/h, HS = 84.91 U/h) improved to levels not significantly different from controls, whereas trypsin (ES = 226.4 U/h, HS = 213.1 U/h; P < 0.03) and acid secretion (ES = 3.52 mEq/h, HS = 11.85 mEq/h; P < 0.01) remained significantly impaired. Severe undernutrition was associated with primary gastric parietal and pancreatic acinar cell dysfunction, which, at least in the case of pancreatic enzymes, appeared to be the determining factor controlling secretion in these patients.

Background: Increased levels of collagen types I, III and V are found in strictures of patients with Crohn's disease (CD) compared with normal gut tissue. Type IV collagen is present in the basement membranes, basal lamina, retina and cornea. Elevated levels of antibody to Klebsiella pneumoniae are found in both active CD and active ankylosing spondylitis (AS) patients compared with healthy controls., Methods: Reactivities for immunoglobulin class-specific antibodies (IgM, IgG and IgA) against collagen types I, III, IV, V and whole K. pneumoniae were measured by ELISA in nine patients with early CD and 10 with late CD from King's College Hospital and 12 late CD patients and 36 HLA-B27-positive AS patients from Middlesex Hospital and was compared with values for 26 healthy controls from the Blood Transfusion Service in London., Results: Levels of class-specific IgM, IgG and IgA antibodies to collagen types I, III, IV, V and K. pneumoniae were significantly elevated in early and late CD patients compared with healthy controls (P<0.001). Levels of IgM, IgG antibody to the four collagen types and K. pneumoniae were also significantly elevated (P<0.001) in AS patients compared with healthy controls. In addition, the level of IgA antibody to K. pneumoniae was elevated in AS patients (P<0.001). Furthermore, a positive correlation between antibody levels to collagen types I, III, IV and K. pneumoniae was demonstrated in both early and late CD patients and in those with AS, whilst a positive correlation to type V was found in early CD., Conclusion: The role of K. pneumoniae and anti-collagen antibodies in the aetiopathogenesis of CD and AS requires further study.

Background & Aims: Prediction of relapse of inflammatory bowel disease has important implications for therapeutic strategies. We assessed whether measurement of intestinal permeability and inflammation could predict relapse of inflammatory bowel disease (IBD)., Methods: Forty-three patients with Crohn's disease (CD) and 37 with ulcerative colitis (UC) in clinical remission provided a stool sample to be assayed for calprotectin (a neutrophil-specific marker), and patients with CD additionally underwent a small intestinal permeability test. Relapse was defined using clinical disease activity indices., Results: Twenty-five (58%) patients with CD and 19 (51%) with UC had a relapse over the 12-month period. Median calprotectin levels in the relapse groups (122 mg/L for CD, 123 mg/L for UC; normal <10 mg/L) differed significantly (P<0.0001) from those of the nonrelapse groups (41.5 mg/L for CD, 29.0 mg/L for UC). At 50 mg/L, the sensitivity and specificity of calprotectin for predicting relapse in all patients with IBD were 90% and 83%, respectively. Permeability in the CD patients who relapsed (median, 0.075; normal <0.04) differed significantly (P = 0. 004) from that in the nonrelapse group (median, 0.038). At the level of 0.05, the sensitivity and specificity of permeability in predicting relapse were 84% and 61%, respectively., Conclusions: Fecal calprotectin predicts clinical relapse of disease activity in patients with CD and UC, whereas small intestinal permeability is a useful predictor of relapse in patients with small intestinal CD.

Inflammatory bowel disease (IBD) is characterized by a chronic relapsing intestinal inflammation. IBD is subdivided into Crohn disease and ulcerative colitis phenotypes. Given the immunologic dysregulation in IBD, the human-leukocyte-antigen region on chromosome 6p is of significant interest. Previous association and linkage analysis has provided conflicting evidence as to the existence of an IBD-susceptibility locus in this region. Here we report on a two-stage linkage and association analysis of both a basic population of 353 affected sibling pairs (ASPs) and an extension of this population to 428 white ASPs of northern European extraction. Twenty-eight microsatellite markers on chromosome 6 were genotyped. A peak multipoint LOD score of 4.2 was observed, at D6S461, for the IBD phenotype. A transmission/disequilibrium test (TDT) result of P=.006 was detected for D6S426 in the basic population and was confirmed in the extended cohort (P=.004; 97 vs. 56 transmissions). The subphenotypes of Crohn disease, ulcerative colitis, and mixed IBD contributed equally to this linkage, suggesting a general role for the chromosome 6 locus in IBD. Analysis of five single-nucleotide polymorphisms in the TNFA and LTA genes did not reveal evidence for association of these important candidate genes with IBD. In summary, we provide firm linkage evidence for an IBD-susceptibility locus on chromosome 6p and demonstrate that TNFA and LTA are unlikely to be susceptibility loci for IBD.

Inflammatory bowel disease (IBD) is characterized by a chronic relapsing intestinal inflammation, typically starting in early adulthood. IBD is subdivided into two subtypes, on the basis of clinical and histologic features: Crohn disease and ulcerative colitis (UC). Previous genomewide searches identified regions harboring susceptibility loci on chromosomes 1, 3, 4, 7, 12, and 16. To expand our understanding of the genetic risk profile, we performed a 9-cM genomewide search for susceptibility loci in 268 families containing 353 affected sibling pairs. Previous linkages on chromosomes 12 and 16 were replicated, and the chromosome 4 linkage was extended in this sample. New suggestive evidence for autosomal linkages was observed on chromosomes 1, 6, 10, and 22, with LOD scores of 2.08, 2.07, 2.30, and 1.52, respectively. A maximum LOD score of 1.76 was observed on the X chromosome, for UC, which is consistent with the clinical association of IBD with Ullrich-Turner syndrome. The linkage finding on chromosome 6p is of interest, given the possible contribution of human leukocyte antigen and tumor necrosis-factor genes in IBD. This genomewide linkage scan, done with a large family cohort, has confirmed three previous IBD linkages and has provided evidence for five additional regions that may harbor IBD predisposition genes.

Background & Aims: Inflammatory bowel disease (IBD) is a complex disorder of unknown etiology. Epidemiological investigations suggest a genetic basis for IBD. Recent genetic studies have identified several IBD linkages. The significance of these linkages will be determined by studies in large patient collections. The aim of this study was to replicate IBD linkages on chromosomes 12 and 16 in a large European cohort., Methods: Three hundred fifty-nine affected sibling pairs from 274 kindreds were genotyped using microsatellite markers spanning chromosomes 12 and 16. Affection status of the sibling pairs was defined as Crohn's disease (CD) or ulcerative colitis (UC)., Results: Nonparametric statistical analyses showed linkage for both chromosomes. Two-point results for chromosome 12 peaked at D12S303 (logarithm of odds [LOD], 2.15; P = 0.003) for CD and at D12S75 (LOD, 0.92; P = 0.03) for UC. Multipoint analyses produced a peak LOD of 1.8 for CD. Chromosome 16 showed linkage for CD at marker D16S415 (LOD, 1.52; P = 0.007). Multipoint support peaked above markers D16S409 and D16S411 (LOD, 1.7)., Conclusions: These data are consistent with linkage of IBD to chromosomes 12 and 16. The replication of genetic risk loci in a large independent family collection indicates important and common susceptibility genes in these regions and will facilitate identification of genes involved in IBD.

Background: The effect of infection by Helicobacter pylori on gastric physiology in duodenal ulcer subjects is controversial. There is evidence that the infection is associated with abnormalities in gastrin homeostasis. Consistent changes in pentagastrin-stimulated acid secretory status have proved difficult to establish. This may be because patients have been studied too soon after Helicobacter pylori eradication., Aims: To study the immediate and longer term effect of Helicobacter pylori eradication on basal and pentagastrin-stimulated acid secretion in duodenal ulcer subjects., Patients and Methods: Patients with active duodenal ulcer disease were studied. Ulcers were healed with sucralfate 2 g bd or ranitidine 300 mg nocte. Helicobacter pylori eradication was attempted with bismuth-based "Triple Therapy", and the nine patients in whom the organism was successfully eradicated were followed and studied over the 12-month period. Acid secretion was studied at entry (prior to the initiation of therapy), following healing, following eradication and 12 months later. Basal, low dose (0.1 microgram/kg) and high dose (6 micrograms/kg) pentagastrin-stimulated acid secretion was determined., Results: Whilst there was a tendency for basal and low dose-stimulated acid secretion to fall following eradication, in this study only the reduction in high dose-stimulated acid secretion achieved significance following eradication (entry mean = 59.6, post eradication mean = 49.6, p < 0.03). This effect of eradication on high dose pentagastrin-stimulated acid secretion was also seen at the 12-month study (mean = 48.9, p < 0.02 versus entry)., Conclusion: The findings of this study suggests that maximally stimulated acid secretion is modestly, albeit significantly, reduced following Helicobacter pylori eradication and that this effect persists.

This article contains a review of the importance and the adverse consequences of patients not receiving information about resuming sexual activity following an acute myocardial infarction (AMI). The available evidence indicates that nurses are failing to supply this form of advice for a number of reasons. Therefore this paper is focused on the development of an information leaflet which can be used as a vehicle for assisting nurses in meeting patients' needs in this area, the content of which may not have been conceived as important or considered at all during the period of the patients' hospitalisation.

105Rh(III)Cl2 complexes with a limited series of [14]ane- and [16]ane- thia macrocycles were prepared and their biodistributions in Sprague-Dawley rats studied. These studies demonstrate that modifications in the structure and composition of the 105Rh-thia macrocycle complexes produce significant differences in their uptake and retention in both the liver and kidneys. The results indicate that the cis-Rh(III)Cl2-[14]ane thiamacrocycles exhibit less kidney retention than the corresponding trans-Rh(III)Cl2-[16]ane thiamacrocycles. In addition, the presence of a side chain containing a carboxylate group will produce decreased retention of activity in the kidneys. HPLC analysis of urine from these animals indicates no observable in vivo metabolism or dissociation of these chelates in the blood stream.

Acid secretory responses and parietal cell sensitivity (PCS) have been studied in 21 duodenal ulcer patients before and after successful treatment with omeprazole (n = 7), sucralfate (n = 7), or Maalox (n = 7). The second study was carried out 3 days after documented healing and withdrawal of treatment in the sucralfate- and Maalox-treated groups and 14 days after documented healing and withdrawal of treatment in the omeprazole-treated patients. Acid output (mmol/hour) was measured as basal secretion, and in response to 0.1 microgram/kg/hour pentagastrin (low-dose) and 6.0 micrograms/kg/hour pentagastrin (high-dose) stimulation. PCS was calculated as the ratio of low dose:high dose acid output (expressed as a percentage). Ulcer healing with sucralfate resulted in significant (p less than 0.05) decreases in low-dose acid output from 36.4% (13.2-51.0) (median [range]) to 8.4% (3.2-45.4) mmol/hour and PCS from 69.1% (44.9-91.4) to 22.0% (16.0-85.6), whereas no significant decreases in any of the measured parameters were noted following ulcer healing with Maalox. Ulcer healing with omeprazole resulted in significant (p less than 0.05) decreases in basal acid output from 6.3 (1.5-22.9) (median [range]) to 2.2 (0-6.9) mmol/hour, and low-dose acid output from 31.0 (6.0-58.0) to 23.0 (1.4-44.8) mmol/hour. These findings suggest that acid secretory responses following ulcer healing vary according to the therapeutic agent used.

Patients with endoscopically proved duodenal ulcer were randomly assigned to treatment with either ranitidine 300 mg at bedtime or sucralfate 2 g twice daily for six weeks. Acid-secretory studies were performed before commencement and 60 to 84 hours after cessation of treatment and endoscopic healing was confirmed. Patients were randomly assigned to receive a constant infusion of secretory stimulant: either pentagastrin 0.1 and 6.0 micrograms/kg/hour or histamine acid phosphate 4.0 and 40 micrograms/kg/hour. Acid output in mmol/hour was measured for basal, low dose, and high dose output. Parietal cell sensitivity (PCS) was calculated as the ratio of low-dose acid output: high-dose acid output and expressed as a percentage. Values before and after treatment were compared and significance of differences was determined using the Student paired t test. There was an apparent decrease in basal acid output, low-dose acid output, high-dose acid output, and PCS with ulcer healing, regardless of treatment or stimulant used. Basal acid output, low-dose acid output, high-dose acid output, and PCS were significantly lower in the sucralfate-treated group, but only high-dose acid output decreased significantly in the ranitidine-treated group. These differences may be relevant to early duodenal ulcer relapse in ranitidine-treated patients.

Intra- and crossmodal performance of normal and retarded readers was compared in a reaction-time task. Both reading groups showed slower crossmodal than intramodal shifting. This effect occurred equally for both reading groups. Differences between the two groups occurred, however, when a complex visual stimulus was present. The complex stimulus resulted in the retarded readers showing slower reaction times to other stimuli in that setting. This effect occurred for stimuli both within and across modalities. The results suggested that the demands of stimulus complexity within the visual modality rather than the demands of crossmodal shifting were related to reading ability.